Abstract
The purpose of the present study was to investigate the influence of afferent activity (mainly homonymous Ia-afferent activity) on the modulation (post-activation depression) of the soleus H-reflex during isolated and passive sinusoidal ankle joint rotations at a speed and amplitude comparable to slow walking. The H-reflex modulation was measured in the relaxed soleus muscle on human subjects during different imposed patterns of 20° haversine ankle joint rotations (0.5–0.6 Hz) while they were sitting comfortably in a chair. Eighteen healthy males and four male patients with clinically complete spinal cord lesion above the soleus motoneuron pool participated in the study. During a single dorsi–plantar flexion rotation the H-reflex was depressed to 27±7% (mean±S.E.M.) of the initial level within 600 ms. The course of this depression was reversed when the dorsi-flexion velocity started to decrease. At the end of the dorsi-flexion movement the depression was already relieved to a level of 73±6% of the initial level. The H-reflex returned more slowly to the initial level within 2 s after the end of the movement cycle. During two consecutive ankle joint rotations and continuous ankle joint rotations both at 0.5 Hz the H-reflex was modulated but also generally depressed while the movement was imposed. The reflex only returned to the reference level after the movements were stopped. These observations indicate the action of a fast and a slow mechanism in the post-activation depression of the soleus H-reflex. The H-reflex modulations observed in the spinal cord injured patients were comparable to the reflex modulations observed in the healthy subjects, except the depressions were smaller. This suggests that a major part of the amplitude of the H-reflex modulation observed in healthy subjects was caused by peripheral and spinal influences. The fast 500 ms recovery of the H-reflex had a time course comparable to presynaptic inhibition. The slow 2 s recovery after the end of a given imposed movement may be explained by a change in the probability of transmitter release from the homonymous soleus Ia-afferent synaptic terminals after repeated activations.
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